Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infective endocarditis caused by Kingella denitrificans occurs rarely. A review of the literature reveals only 6 cases of endocarditis caused by the bacillus. K. denitrificans is normally a commensal of the upper respiratory airways, may exceptionally be responsible for endocarditis. A case of possible prosthetic endocarditis caused by K. denitrificans is presented. A 78-year-old male with Type II diabetes was admitted to the hospital complaining of fever, a sore throat and arthralgia. He underwent replacement surgery of a St. Jude medical prosthesis for aortic stenosis at the age of 75. The only physical findings at admission were a temperature of 38.2 degrees C and murmurs of mild mitral regurgitation. The liver and spleen were not palpable, and there were no skin or eye lesions. Laboratory findings were as follows: white blood cell count 9500/microliters with 77% neutrophils, erythrocyte sedimentation rate 71 mm/h (Westergren), blood urea nitrogen 50.2 mg/dl, serum creatinine 1.7 mg/dl and C-reactive protein 22.2 mg/dl. The Gram-negative bacillus isolated from the blood was identified as K. denitrificans by the identification system, namely ID test.FN-20 rapid (Nissui, Japan). Although an echocardiogram detected no vegetation, infective endocarditis was diagnosed because the same bacillus was detected by separate blood cultures and an obvious source of infection was not found other than the prosthetic valve. Initial treatment was flomoxef, which was changed to Ampicillin 2 g/day after K. denitrificans was identified. Ampicillin continued for 6 weeks. The clinical course was good and he did not require further surgery. He has been afebrile for 2 years after completing treatment. This case represents the first report of prosthetic valve endocarditis caused by K. denitrificans in Japan.
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PMID:[Prosthetic endocarditis caused by Kingella denitrificans in a patient with diabetes mellitus]. 928 46

Genetic haemochromatosis (GH) is one of the most common hereditary diseases, with a prevalence of 1-5/1000 in the Western world. In 90 per cent of cases a mutation is found in an MHC-class-like gene designated HFE, involving a substitution at position 282 of the HFE protein and resulting in defective binding of beta(2)-microglobulin. Animals with beta(2)-microglobulin deficiency develop iron overload, indicating this protein to be involved in the regulation of iron metabolism. Hepatic iron overload results in increased production of oxygen free radicals and peroxidation of membrane lipids, thus causing damage to lysosomes, mitochondria and the endoplasmic reticulum. These cellular events may progress to cell death, fibrogenesis, and the development of liver cirrhosis which is associated with a 200-fold increase in risk of hepatocellular carcinoma. In addition to the risk of diabetes, arthralgia, cardiac arrhythmia, pituitary insufficiency and hypogonadism, iron excess is also associated with aggravation of the cytotoxic effects exerted on hepatocytes by other agents such as alcohol or hepatotrophic viruses. The treatment of iron overload in GH consists of weekly venesection until the serum ferritin level is normalized, followed by maintenance therapy. Survival rates are normal if the disease is detected and treated before complications have developed.
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PMID:[Defective iron metabolism in genetic hemochromatosis. The mechanisms remain unknown in spite of genetic advances]. 972 62

Chronic fatigue, arthralgia, infertility, impotence, cardiac disease, diabetes and abnormality of liver enzymes could point to the presence of haemochromatosis. A patient with one of these symptoms, a normal haemoglobin content, but an increased transferrin saturation and serum ferritin level most probably has a primary haemochromatosis. Most primary haemochromatoses have a genetic background. The diagnosis 'HFE-related haemochromatosis' is made when a homozygous Cys282Tyr mutation is found in the HFE-gene. However, in approximately 10% of the patients with the clinical features of primary haemochromatosis this mutation is absent. The treatment of primary haemochromatosis consists of regular phlebotomy. Liver biopsy is indicated if fibrosis, cirrhosis or another hepatic disease is suspected. Family screening of first-grade relatives is indicated for all patients with primary haemochromatosis.
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PMID:[Diagnosis and treatment of primary hemochromatosis]. 1042 53

We report a case of cutaneous tuberculosis presenting as cellulitis. The patient was a 63-year-old Korean woman who also had diabetes mellitus and a 20-year-history of oral corticosteroid medication prescribed for arthralgia. In addition, she had had pulmonary tuberculosis 20-year previously for which she received systemic treatment for 1 year. Her clinical cellulitis failed to respond to antibiotic therapy. Subsequent investigations, using histopathology and polymerase chain reaction, established an alternative diagnosis of cutaneous tuberculosis. The skin eruption cleared after treatment with isoniazid, rifampicin, ethambutol and pyrazinamide. This case represents a most unusual presentation of tuberculosis in the skin. The atypical features may reflect the patient's general medical state.
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PMID:Tuberculous cellulitis. 1084 1

Genetic hemochromatosis is an autosomal recessive disease, characterized by an increased iron absorption, leading to progressive iron overload. The fully expressed phenotype comprises fatigue, skin pigmentation, liver disease with hepatomegaly, cirrhosis and hepatocellular carcinoma, and diabetes. Arthralgias are frequent, cardiopathy or impotence may occur. This presentation is now unfrequent with earlier diagnosis, and patients are often asymptomatic--with only biochemical expression--or pauci-symptomatic (mild fatigue, arthralgias or increased transaminases). Transferrin saturation is always increased. Serum ferritin is proportional to iron burden. Diagnosis is now easy, since most patients are homozygote for the C282Y mutation of the HFE gene. Liver biopsy can be useful to quantify iron overload and assess liver fibrosis. The disease can be lethal due to liver disease, carcinoma or heart disease, but life expectancy goes to normal if patients are treated before the occurrence of cirrhosis. Treatment relies on regular venesections. Familial screening is essential.
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PMID:[Diagnosis and treatment of genetic hemochromatosis]. 1086 97

Genetic hemochromatosis (GH) is a late-onset, autosomal recessive disorder. The majority of those at risk from iron overload and its clinical consequences may be detected by a simple genetic test. Furthermore, treatment by phlebotomy, if instituted early, removes excess iron and prevents the complications of iron overload which include arthralgia, diabetes, and cirrhosis of the liver. GH seems to be an obvious candidate for inclusion in national screening programs. However, important questions remain concerning the proportion of individuals with the high-risk genotype who eventually show clinical manifestations of iron overload and the significance of heterozygosity for haemochromatosis in terms of morbidity. Until these questions are resolved, the introduction of widespread genetic screening cannot be justified.
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PMID:Early detection of genetic hemochromatosis: should all young adults be offered the genetic test? 1095 63

We report a case of long-standing SLE which presented with symptomatic muscle vasculitis on a background of photosensitivity, arthralgia and myalgia. The diagnosis was complicated by cardiomyopathy, nephrotic syndrome and diabetes. We highlight the benefits of aggressive treatment in severe disease and the importance of recognising and treating comorbidity especially ih relation to atherosclerosis.
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PMID:A swollen leg unmasks longstanding SLE. 1124 6

We studied 21 patients with septic arthritis of the sternoclavicular joint at Chulalongkorn University Hospital between January 1987 and January 1997. There were 15 males (71.4%) and 6 females (28.6%). The mean age was 47.4 years with a range of 16 to 69. More than half of the patients (57.1%) were aged more than 50 years and most had associated diseases including diabetes mellitus and cirrhosis. Almost all of the younger age group had a history of intravenous drug abuse. All of the patients had fever and sternoclavicular joint pain. Most of the patients (66.7%) had monoarticular arthritis, whereas, the others had oligoarticular arthritis. Staphylococcus aureus was the most commonly or identified organism in the patients. Retrosternal abscess was seen by computerized tomography in 6 patients (28.6%). All patients received parenteral antibiotics, and 5 patients (23.8%) required surgical drainage of a retrosternal abscess. Eighteen patients recovered but there were 3 (14.3%) deaths. All of these had retrosternal abscesses. The major cause of death was septic shock. Septic arthritis of the sternoclavicular joint is an uncommon disease in Thai clinical practice. Although uncommon, retrosternal abscess is a life threatening complication.
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PMID:Clinical features of septic arthritis of sternoclavicular joint. 1128 2

Diabetic muscle infarction is a rare complication of diabetes and has characteristic clinical features including acute onset of pain with painful swelling, most commonly in the thigh or calf muscle, which gradually improves to complete resolution. Recently we experienced a case of diabetic muscular infarction presenting as knee joint pain due to involvement of the proximal portion of the leg muscle, which site has not been reported previously. This case shows that diabetic muscle infarction may involve sites other than the thigh and calf areas and should be considered in the differential diagnosis of knee arthralgia.
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PMID:Case report: diabetic muscle infarction presenting as knee arthralgia. 1167 1

In numerous studies of symptoms in patients with chronic hepatitis C there has been no systematic assessment of both fatigue and extrahepatic manifestations. Our objective was to assess the prevalence of fatigue in patients with hepatitis C virus (HCV) infection, and to identify associations between fatigue and clinical and biological hepatic and extrahepatic manifestations. We studied 1614 patients. Data were prospectively recorded during the first visit of patients infected with HCV and the prevalence of fatigue and its association with dermatological, rheumatological, neurological and nephrological manifestations; diabetes; arterial hypertension; auto-antibodies, and cryoglobulinaemia were assessed. Then, using multivariate analysis, we identified demographic, biochemical, immunological, virological, and histological factors associated with the presence of fatigue. Fatigue was present in 53% of patients (95% confidence interval 51-56). In 17% of patients (95% confidence interval 15-19) fatigue was severe, impairing activity. Five other extrahepatic manifestations had a prevalence above 10% including, in decreasing order: arthralgia, paresthesia, myalgia, pruritus, and sicca syndrome. In univariate and multivariate analyses, fatigue, in comparison with the absence of fatigue, was associated with female gender, age over 50 years, cirrhosis, depression and purpura. Independent of these associations, fatigue was associated with arthralgia, myalgia, paresthesia, sicca syndrome and pruritus. The prevalence of fibromyalgia (as defined by the association of fatigue with arthralgia or myalgia) was 19% (95% confidence interval 17-21). There was no significant association between fatigue and the following characteristics: viral load or genotype, alcohol consumption, abnormal thyroid function, and type and level of cryoglobulinaemia. Hence, fatigue is the most frequent extrahepatic manifestation in patients infected with HCV. Fatigue is independently associated with female gender, age over 50 years, cirrhosis, depression and purpura.
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PMID:Fatigue in patients with chronic hepatitis C. 1208 7


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